Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The etiopathogenesis of ulcer disease is comprehensive and many experimental and clinical data failed to prove the primary cause of the disease. Although much has been learned concerning the pathophysiological mechanism which appear important in the development of ulcer disease, our present knowledge of the etiology of this disease is incomplete. Depression of the gastric acid secretion still remains the main treatment approach, although the cytoprotective drugs are interesting therapeutic challenge. Etiology of the peptic ulcer disease is not solved yet, but the defense mechanisms of the gastric mucosa are much more clear what will lead to better understanding of the defense mechanisms in the gastric cancer. Omeprazole is an interesting new drug healing peptic ulcer in almost 100% of the patients. A philosophic question may be asked: "Do we need to know the etiology of the disease in order to be able to treat it properly?" Omeprazole heals the ulcer and, in fact, we do not know its etiology. In the cost-benefit ratio, the most widely used drugs are still H2-receptor antagonists and sucralfate, and omeprazole is reserved for the patients with resistant ulcer disease, Zollinger-Ellison syndrome and severe reflux esophagitis.
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PMID:[New findings in the etiopathogenesis of ulcers and reevaluation of therapy]. 196 Oct 77

We examined the effect of proton pump inhibitor omeprazole on neuromuscular paralysis induced with either nondepolarizing or depolarizing neuromuscular blocking drugs in anesthetized and mechanically ventilated rats. Neuromuscular paralysis, as judged by tibialis anterior muscle twitch tension in response to sciatic nerve stimulation, was maintained at about 50% with intravenous (i.v.) bolus and infusion regimens of either atracurium or succinylcholine. Omeprazole, 0.5, 1, and 10 mg/kg i.v., was then administered at 10-min intervals while the infusion of the neuromuscular blocker was continued. Omeprazole at all three doses increased the steady-state neuromuscular paralysis produced with either atracurium (pre-omeprazole versus final post-omeprazole paralysis; mean +/- SE, n = 6, 53.0% +/- 2.3% vs 80.0% +/- 5.3%) or succinylcholine (50.8% +/- 1.5% vs 86.4% +/- 5.1%). Omeprazole, 0.5, 1.0, and 10 mg/kg i.v., given directly and without any neuromuscular blocker, produced approximately 5% depression of the muscle twitch response. Omeprazole, i.v. at human therapeutic doses, alters neuromuscular function and enhances the action of both atracurium and succinylcholine in vivo in rats.
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PMID:Omeprazole potentiates atracurium and succinylcholine paralysis in vivo in rats. 810 72

The effect of omeprazole (2 mg kg-1 i.v.) on respiratory depression induced in rats by acute oral methadone administration (5 mg kg-1) was examined and compared with control animals that only received methadone. Quantitative assessments of arterial Pco2,Po2, pH, and respiratory rate were employed as criteria for evaluation. Intragastric pH was measured in each rat immediately before and 2 h after methadone. Plasma concentration of methadone was measured for 3 h. The relationship between drug effect and the systemic bioavailability of methadone, measured as the area under the plasma concentration-time curve (AUC0-180), was also evaluated. The intensity of the methadone-induced respiratory depression was significantly greater in the omeprazole group than in control rats. A significant variation (p < 0.01) in all respiratory parameters was detected from 30 to 120 min after methadone. Omeprazole caused a significant increase in methadone levels (Cmax = 156 +/- 6.5 ng mL-1 against 51 +/- 5.8 ng mL-1 in control; p < 0.05). AUC0-180 was higher (p < 0.05) after omeprazole treatment (18.6 +/- 1.4 micrograms mL-1 min) than in control (6.8 +/- 0.6 microgram mL-1 min). Two hours after treatment with omeprazole, intragastric pH values were significantly elevated (4.7 +/- 0.1 against 2.2 +/- 0.04) and continued increasing, being 6.4 +/- 0.1 at the end of the experiment. Correlation was observed between intragastric pH and the area under the effect- (respiratory depression-) time curve (r = 0.74; p < 0.001). A relationship between plasma methadone levels at 120 min and gastric pH (r = 0.92; p < 0.001) was detected. A significant correlation between the area under the effect-time curve (0-120 min) and AUC0-180 has been also observed (r = 0.90; p < 0.01). These pharmacokinetic and pharmacodynamic changes could be gastric pH dependent because they were mimicked when gastric pH was experimentally modified by bicarbonate whereas opposite results were obtained with acidic pH2 solution.
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PMID:The effect of changes in gastric pH induced by omeprazole on the absorption and respiratory depression of methadone. 889 14

A 91-year old female presented to Acute Medical Unit with a 2 week history of shortness of breath and haemoptysis. Her past medical history included osteoporosis, depression, irritable bowel syndrome, asthma, cataracts, and a colonic polypectomy. Her medications: Citalopram 10 mg, Co-codamol, Beclomethasone 200 mcg inhaler, Salbutamol MDI inhaler, Omeprazole 20 mg and Alendronic acid. She was an ex-smoker with a 20-pack year history who had stopped smoking 40-years ago. She did not drink alcohol and lived alone independently.
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PMID:A Chest X-Ray causing confusion. 3112 1